What I talk about in my daily neurology team rounds

Pontine myelinolysis

We’ve been covering a lot of basics lately in our attending rounds, so there hasn’t been much activity on this blog. Yesterday we spoke about the pathophysiology of resodiumization and how to do it correctly in order to avoid central pontine or extrapontine myelinolysis.

As far as I know, there have been plenty of case reports but not really much development in demyelination syndromes, so that the old review in JNNP is still the best to read. There is a more recent review, though that doesn’t add anything.

My personal view is that we spent too much time on Na-cosmetics and forget about the complexities of electrolyte and osmotic homeostasis. So I recommend analyzing your HypoNa-panel (serum/urine pairs of Na, K, Cl, osmolality, uric acid) with one of your favorite algorithms, before acting.

(Unless, of course, the patient is in immediate vital danger, i.e. in status epilepticus with hyponatremic brain edema, in which case you simply substitute harshly with about 50ccs of very high sodium solution (take bicarb if chloride is high, otherwise 3% or 7,4% NaCl), rechecking Na every few minutes with your blood gas analysis.)

Chloride, phosphate, Mg, Ca – all these seem vitally important to me when contemplating to elevate Na slowly. Also, don’t forget to provide nutrition as early as possible, because for osmobalance oligodendrocytes need amino acids.

If Na spikes too fast, block diuresis with DDAVP, then control fluid and Na balance yourself (since the kidney doesn’t seem to be able to do it) as described in Sterns‘ approach.

When CPM or EPM happened and you recognize it early, there is some hope of reversing, pushing Na down to 128-130 mmol/l for 2 days, before slowly letting it return.

Don’t expect any prognostic value from neurophysiological examinations or MRI.